PRTN3 and rheumatoid arthritis: In keeping with the aforementioned studies on the different gene–environment interactions in RF-positive and ACPA-positive patients [34,35,36], these results would suggest that pulmonary inflammation could favor RA development not only through the formation of neo-antigens, but also via a number of other mechanisms, such as cytokine production, T cell polarization, epigenetic changes, modulation of the local microbiome, and others [45].